Project/Area Number |
24590868
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Legal medicine
|
Research Institution | St. Marianna University School of Medicine |
Principal Investigator |
KANNO Sanae 聖マリアンナ医科大学, 医学部, 助教 (50391090)
|
Co-Investigator(Renkei-kenkyūsha) |
HIRANO Seishiro 国立環境研究所, 室長 (20150162)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | NLRP3 inflammasome / Rho-kinases / Interleukin 1beta / THP-1 cells / Fibrous particles / Interleukin-1beta / ナノマテリアル / 暴露 / インフラマソーム / Rho-kinase / アスベスト / 生体影響 |
Outline of Final Research Achievements |
Long fibers, such as asbestos and carbon nanotubes (CNTs), are more potent activators of inflammatory and genotoxicity than short or tangled fibers. Fibrous particles trigger interleukin-1beta secretion and cause inflammatory diseases through NLRP3 inflammasomes in phagocytotic cells. This study clarified that GTPase effector Rho-kinases (ROCK1, and 2) are involved in inflammasome responses induced by fibrous particle, such as asbestos, CNTs and monosodium urate in THP-1 cells. Though further study is required to elucidate the function of ROCKs on NLRP3 inflammasomes activated by fibrous particles, present findings suggest that ROCKs inhibitor might directly or indirectly abrogate NLRP3 inflammasomes, leading to several autoinflammatory diseases triggered by fibrous particles. I examined To clarified the mechanism of NLRP3 inflammasomes induced by fibrous particles.
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